Below is an important statement from Prof Terje Traavik, the text of which is reproduced in full from a pdf which can be sent to anyone who would prefer to receive it in its original format.
First some introductory comments from Dr Ignacio Chapela from whom we received this.
(For more statements about GM by scientists see: http://www.gmwatch.org/p1temp.asp?pid=3&page=1)
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Dear colleagues,
Perhaps some of you did not register the recent flare of internet news and counternews epicentered from Kuala-Lumpur. Following a presentation by Terje Traavik to the forum of scientists, regulators, civic groups and individuals gathered for the Biodiversity Convention meetings, we were all bracing for a new round of the now common pattern of (a) scientific news followed by (b) discredit, followed by (c) silence, followed by (d) business-as-unusual as always these days (cf the first seven minutes of the webcast http://nature.berkeley.edu/pulseofscience).
Not this time. I want to share with those who might not have received it, a document which is perhaps the most important science writing in the last quarter century - a span of time convenient to my ignorant mind since it matches the rough age of the Bioteck Rev.
I invite you to read Terje's own words, which carry the pregnancy of our dire times seen through the transparent lens of Tromsø, 70 degrees N Latitude. If nothing else, I expect we will all be engaged with this document for years to come, in its own way a break of silence.
Of course it is not a coincidence that these words would be coming to us in tandem with Bruno Latour's own retraction of sorts, his spitting at "critical barbarity", his call to move from matters-of-fact to matters-of-concern (cf Critical Inquiry, or better edited, Harper's).
Bruno tracking Terje?
With regards,
Ignacio
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A response to criticism about our work on GE biosafety.
The Cartagena protocol, the Precautionary principle, "sound science" and "early warnings".
Terje Traavik, Dr. philos.
Scientific Director, GENØK-Norwegian Institute of Gene Ecology
Professor of Gene Ecology, University of Tromso
Background
On February 22, 2004, I presented the results of ongoing research at the Biosafety Symposium in Kuala Lumpur, held just prior to the first Meeting of the Parties on the Cartagena Protocol on Biosafety. The Symposium was jointly organised by the Third World Network (a science-interested organisation), the Norwegian Institute of Gene Ecology (GENØK) and the New Zealand Institute of Gene Ecology.
The Symposium was accessible to the public, but it was primarily a meeting for those with professional interests in biosafety.
The presentation of our preliminary research findings was done in the spirit of the greatest of traditions to share the results of research among peers. This tradition has dominated the biological sciences for centuries. Possibly that tradition has become difficult to recognise in an age when most research is filtered for information that must be kept secret for commercial or other reasons. I am proud and grateful to be supported by public agencies who impose no such requirements.
Speaking now for the two Institutes of Gene Ecology, we also reject any inclination among particular parties to define our peer group. The Institutes of Gene Ecology are organised on the principle that bio-applications will have impacts on the planet and the ecology of human beings that transcend dated and arbitrary notions of where biology ends and ethics, social science, law, economics, philosophy and culture begin. Our peer group is composed of those who are specialists in the impacts of genetically engineered organisms.
As a community we have a membership that covers all traditional research backgrounds mentioned above. More importantly, each individual among us has a commitment to understand what can be learned from all those disciplines when focused on a single issue - genetically engineered organisms.
That latter quality opens our minds to the bodies of knowledge held in non-traditional sources. By this we mean both NGOs and the industry. Our peer group and our emerging competence in holistic impact assessment is what we believe make us unique.
I have been criticised for speaking about my research at the Kuala Lumpur Biosafety Symposium. This is an insult to the audience which was composed of respected scientific specialists, members of the competent regulatory community, and accomplished researchers of the many disciplines whose interests intersect the impacts of new bioapplications, including genetically engineered organisms.
Cartagena Protocol
The Precautionary Principle plays an important role in the Cartagena Protocol, an international agreement on transboundary movement of GMOs (www.biodiv.org/biosafe/protocol), and in regulations, i.e. the Norwegian Gene Technology Act of 1993 (www.bion.no) and EU directive 2001/18/EC(www.europa.eu.int/comm/food/fs/sc/scp/out31_en.html). The Precautionary Principle instructs us to anticipate the potential hazards of genetic engineering applications.
Employment of the Precautionary Principle (PP) entails identification of risk, scientific uncertainty and ignorance, and involves transparent and inclusive decision-making processes (Freestone and Hey, 1996). Although a tool for policy decision, I will claim that implementation of the PP must have impact on the research agenda. Employment of the PP emphasises the importance of scientists taking responsibility for anticipation, acknowledgement and communication of uncertainty, in order to produce scientifically and socially robust knowledge (Myhr and Traavik, 2003).
In a very real sense, the spirit of Cartagena, perhaps uniquely, gives the environment legal standing and places the burden-of-proof of safety on those who might damage her. I favour application of a strong version of the PP, realizing the need to identify and acknowledge scientific uncertainty related to GE applications before they are commercialised. The future of mankind and the environment is inter-dependent. Damage to ecosystems and other species will also hurt mankind in the long run. Pure anthropocentric world views may be suicidal for the human species.
When I agreed to speak at the Biosafety Symposium, I fully understood the ethical dilemmas facing scientists when potential "early warnings" of harm to health and the environment appear in their own research. Raised a traditionalist, I began my talk by stating my respect for peer-review as an integrated and necessary part of "sound science" and I of course believe in it. In fact, I believe in it so strongly that I have always, and intend to always, place my work before the entire world, not just before the competent regulatory authorities with restrictions on discussing the content of my findings. This includes early warning reporting. Such reports are necessary to inform other scientists and regulators, giving them the opportunity to "anticipate and prevent", and should be followed up by further research to reveal the validity of the warnings (reports.eea.eu.int/environmental_issue_report_2001_22/).
Peer review itself does not make a scientific finding either true or false. Peer review is neither a single event. Many peer-reviewed publications include the results of research previously tested in a seminar or conference before a critical audience, and before that in a grant application. Grant applications also often contain summaries of preliminary findings. This provides some confidence to granting agencies and their reviewers. The critical audiences alerted to your work during seminars may also begin the process of being inspired to reproduce or extend your findings in ways your imagination has not even considered. That is the process we foster in the professional community; not the process of secrecy.
When it comes to the environment and human health, I strive for nothing less than the most stringently conducted and reported science. That standard is not compromised because some warnings of potential hazard are notified to the competent community through the means discussed above, and early warnings do not preclude the work being subjected to further review as it progresses through to eventual publication in a peer-reviewed journal, often many months in the future.
By similar token, early insight into the commercialisation potential of a research finding would also not await publication in a peer-reviewed journal before a patent application was lodged. The patent is therefore based on observations and tests that have never been openly reviewed, yet applications protected by patents are no less prone to cause concern among the public and governments.
What was the research presented in Kuala Lumpur?
In my talk, in order to illustrate what I meant by "early warnings", I very briefly summarized results from three on-going, long-term projects at GENØK:
*Feeding experiments in rats
*Antibody analyses of sera from Philippine farmers
*Safety aspects of transgenic poxvirus-vectored vaccines
The second item, sera from farmers, has attracted the greatest interest so I will briefly summarise those findings below.
We have used direct and inhibitory ELISAs (enzyme-linked immuno-sorbent assays) to demonstrate IgA, IgG and IgM antibodies specifically binding to Bt-toxin Cry1Ab in sera from Philippine farmers. A general interpretation would be that the farmers had been exposed, in an immunologically meaningful way, to Cry1Ab, or an antigen sharing epitopes with Cry1Ab, during the last 6-9 months before blood samples were taken. This might indicate coincidence in time between three observed events: the very first pollination season for Bt-transgenic maize, an outbreak of respiratory/intestinal disease among individuals living close to the Bt-maize field, and the production of serum antibodies.
I strongly emphasized that the tests could not establish any cause-effect relationships between the 3 events, neither could the results preclude such relationships, and hence they might represent an early warning. As I said at the time, even if I had been able to present the detection of specific anti-Cry1Ab IgE antibodies, my conclusions would have been the same. Why have these results, among many thousands of scientific results presented at conferences annually, attracted so much attention?
These results could challenge long-standing claims based on many unpublished or not peer-reviewed research conducted over the years.
1. *Cry1Ab is not immunogenic*. The bacterial version of Cry1Ac shares antigenic 'epitopes' with Cry1Ab. Since Cry1Ac is strongly immunogenic in rodents, a fact backed up by a series of peer-reviewed articles (e.g. Moreno-Fierros et al 2002; Vazquez et al. 1999, Vazquez-Padron et al., 2000), it is a fair hypothesis that Cry1Ab could inspire an immunological response. Also, Bacillus thuringiensis spraying has elicited specific Cry1A antibodies in farm workers, within the same classes we detected, as well as allergy-related IgE antibodies. These findings were published already in 1999 (Bernstein et al., 1999). There is a distinct difference between being "allergenic" and "antigenic"/"immunogenic": all that is immunogenic is not allergenic.
However, immunogens invoke an immune response and any immune response should be further investigated for being indicative of a potential allergic response.
I am aware of no evidence in the existing peer-reviewed literature that demonstrates that these proteins are neither allergenic nor immunogenic. I am aware of claims that the linear amino acid sequence of the Cry proteins is not similar to any known allergens, but this again is controversial (i.e. Kleter and Peijnenburg, 2002)
Furthermore, that type of evidence has never been evaluated as predictive of proteins that will turn out to not be allergens (Metcalfe, 1996; Stickler et al. 2003).
Moreover, the engineered plant versions of Cry proteins are C-terminally truncated compared to the bacterial protoxins. New epitopes may be created in plants due to new alternative posttranslational modifications and folding of the protein, or on the basis of complexing between the transgene product and endogenous protein(s).
Indeed, most antibodies produced by an allergic individual to inhalant allergens appear to be toward discontinuous epitopes, but it is unknown whether this applies to antibodies to food allergens (Taylor and Lehrer, 1996). These are "sound" scientific hypotheses yet to be experimentally tested, which they should have been before commercialisation of Bt-transgenic plants.
2. *Pollen does not express the cry1ab gene*. This may be true, but if it is it needs to be verified rigorously. By that I mean it must be measured in all engineered plants, it must be measured in plants grown at all sites, and it must be measured for plants grown under different physiological conditions, for a start. The claim should also be made only after corroboration via a number of complementary techniques, e.g. antibody screening of pollen and microarray analysis. This is because eukaryotic promoters, in this case the 35S CaMV promoter used to drive the expression of the gene, can be inactive in one specific environment, for instance somewhere in the US, but there is not absolute reason for it to not be activated in other environments.
To my knowledge, there are no data proving promoter silence in pollen of any Bttransgenic maize variety, and some data to the contrary. For example, for MON 810 corn grown in the U.S., the concentration of Cry was low but detectable (< 90ng/g total protein) (U.S. EPA Bt crop reassessment data).
How much is too little to inspire an allergic reaction? There is currently no lower threshold for sensitization to allergens as far as I know, and certainly not food allergens, although very low concentrations make sensitization less likely . Furthermore, when Bt crops were assessed for allergenicity by the US, they were not carried out according to the best recommended methods (FAO/WHO), undermining confidence in that evidence. The regulatory assessment also assumed sensitization only via oral exposure, not possible respiratory exposure.
Conclusion
The Biosafety Protocol's main objective is to regulate the trans-boundary movement of genetically engineered organisms for purposes of protecting human and environmental health. In the spirit of the Protocol, that capacity must be relevant to the special or unique concerns of the importing nations and their environments.
It is broadly recognized that third world nations are a huge global repository of biodiversity, local knowledge and cultural treasures, much of it yet to be described. Since at present most genetically engineered organisms originate in the first world nations, their movement to other ecosystems must proceed only with the consent of the fully informed citizenry of these nations. With yet-to-be determined impacts of genetically engineered organisms on biodiversity and human health, many species as well as cultures could be at risk from international movements of these organisms. In addition, since most genetically engineered organisms are imported along with first world co-technologies (such as certain agricultural practices, pesticides, herbicides, etc.), trans-boundary movement of genetically engineered organisms could threaten various cultures.
Astute observers of genetically engineered organisms cannot help but recognize that the limitations of biosafety infrastructure are not limited to third world countries, but are a result of a global under-investment in science-for-safety. In this regard, the two Institutes of Gene Ecology are optimistic that this is only the beginning of a sustained effort to raise global awareness and capacity in biosafety. In fact, that biosafety is the priority of the third world is an interesting testimony to the fact that priority investment in science-for-sale does not suit all cultures and is exposing significant gaps even among wealthy nations.
Norway should also be proud that it has taken a leadership position in championing and resourcing the call for science-for-safety as the world's newest priority.
Literature cited
Bernstein, I.L, Bernstein, J.A., Miller, M., Tierzieva, S. et al. 1999. Immune responses in farm workers after exposure to Bacillus thuringiensis pesticides. Environmental Health Perspectives 107: 575-582
CBD: Cartagena Protocol on Biosafety ( http://www.biodiv.org/biosafe/protocol)
EEA: European Environment Agency (2002): Late lessons from early warnings. The precautionary principle 1896-2000 (http://reports.eea.eu.int/environmental_issue_report_2001_22/)
European Council Directive 2001/18/EC (http://www.europa.eu.int/commm/food/fs/sc/scp/out31_en.html
Freestone, D. and Hey, E. (1996): Origins and development of the precautionary principle, in Freestone, D. and Hey, E. (ed.), The precautionary principle and international law (Netherlands: Kluwer Law International), p.3-15.
Gene Technology Act 1993. The act relating to the production and use of genetically modified organisms. Act no. 38 of 2 April 1993, Oslo. http://www.bion.no/biotech_regulations_eng.shtml
Kleter, G.A. and Peijnenburg, AACM. 2002. Screening of transgenic proteins expressed in transgenic food crops for the presence of short amino acid sequences identical to potential IgE-binding linear epitopes of allergens. BMC Structural Biology 2:8
Metcalfe, D.D., J.D. Astwood, R. Townsend et al. 1996. Assessment of the allergenic potential of foods derived from genetically engineered crop plants. Crit. Rev. Food Sci. Nutr. 36(S): S165 S186.
Moreno-Fierros, L., Garcia, N., Lopez-Revilla, R., Vazquez-Padron, R.I. 2000. Intranasal, rectal and intraperitoneal immunization with protoxin Cry1Ac from Bacillus thuringiensis induces compartmentalized serum, intestinal, vaginal and pulmonary immune responses in Balb/c mice. Microbes and Infection 2: 885-890
Myhr, A.I., Traavik, T., 2003. Genetically modified crops: Precautionary science and conflicts of interests. JAGE 16, 227-247.
Stickler M., Much, J., Estell, D., Power, S., Harding, F. 2003. A human dendritic cellbased method to identify CD4+ T-cell epitopes in potential protein allergens. Environmental Health Perspectives 111: 251-254
Taylor, S.L., S.B. Lehrer. 1996. Principles and characteristics of food allergens. Crit. Rev. Food Sci. Nutr. 36(S): S91 S118.
Vazquez, R.I., Moreno-Fierros, L., Neri-Bazan, L., de la Riva, G.A. 1999. Bacillus thuringiensis Cry1Ac protoxin is a potent systemic and mucosal adjuvant. Scand J. Immunol. 49: 578-584
Vazquez-Padron, R.I., Moreno-Fierros, L., Neri-Bazan, L., et al. 2000. Characterization of mucosal and systemic immune response induced by Cry1Ac protein from Bacillus thuringiensis HD 73 in mice. Braz. J. Med. Biol. Res. 33: 147-155